What Is GHRP-2?
GHRP-2 (His-D-Trp-Ala-Trp-D-Phe-Lys-NH2) is a synthetic hexapeptide and one of the most extensively studied growth hormone releasing peptides (GHRPs), with human pharmacokinetic data, pediatric short-stature trials, and adult studies on GH pulsatility, appetite, and anti-catabolic effects. It acts as a potent agonist at the GHS-R1a ghrelin receptor, stimulating robust short-burst GH release from pituitary somatotrophs while suppressing somatostatin tone. GHRP-2 has a short plasma half-life of approximately 30–40 minutes with a GH pulse peaking around 20–40 minutes post-injection, making it well-suited for pulsatile GH protocols. It is commonly paired with GHRH analogs such as CJC-1295 (no DAC) or Sermorelin for synergistic GH axis support.
Quick Reference
Member reference tables summarize the compound's research parameters.
Key Benefits
- Potent, short-burst GH release via GHS-R1a agonism — GH peak within ~25 minutes post-injection, fully cleared within a few hours
- Synergistic with GHRH analogs (CJC-1295 no DAC, Sermorelin) — dual-pathway activation produces substantially larger GH pulses than either peptide alone
- Anti-catabolic in skeletal muscle — directly attenuates Atrogin-1 and MuRF1 ubiquitin ligase expression, reducing proteolysis in catabolic states
- Orexigenic signaling via ghrelin receptor — increases food intake, making it a research tool for appetite regulation and cachexia models
- Among the best-characterized GHRPs in published human pharmacokinetic literature
Mechanism of Action
GHRP-2 binds GHS-R1a at both the pituitary (amplifying GH release from somatotrophs and dampening somatostatin tone) and hypothalamus (influencing appetite and energy balance via ghrelin-responsive neurons). Downstream pituitary effects drive increased GH secretion with subsequent IGF-1 elevation after repeated pulses. In peripheral skeletal muscle, GHRP-2 acts via ghrelin receptors to reduce Atrogin-1 and MuRF1 mRNA expression — the muscle-specific ubiquitin ligases responsible for proteolysis in catabolic states — while stimulating protein synthesis pathways. Notably, GHRP-2 does not significantly alter myostatin mRNA expression, distinguishing its anti-catabolic mechanism from myostatin inhibitors. Short plasma half-life (~33 min IV in pediatric PK study) means each injection creates a discrete, rapid GH pulse rather than sustained elevation.
Research Indications
Research Protocols
As reported in cited literature and research-community logs (see Research Citations below), not a personal dosing recommendation.
This member section describes parameters reported in the research literature.
Peptide Interactions
This member section summarizes reported compound interactions and evidence limitations.
Safety Notes
Included for harm-reduction awareness only, in the event this compound is encountered outside its labeled research use. Inclusion here does not imply RUO Codes endorses, recommends, or instructs human use.
This member section discusses research safety considerations and uncertainties.
Quality Indicators
Reported Research Time Points
This member section summarizes reported research time points.
Research Citations
- Laron Z et al. Growth hormone releasing activity of growth hormone-releasing peptide-2 in children with familial short stature. Acta Paediatrica. 1995.
- Muller EE et al. GHRP-2 and growth hormone secretion: pharmacological and clinical studies. Endocrine. 1999.
- Porporato PE et al. Acylated and unacylated ghrelin decrease muscle atrophy markers in rodent models of cancer cachexia. J Cachexia Sarcopenia Muscle. 2013.
- Garcia JM et al. Ghrelin and its analogs: a systematic review of appetite-related and anti-catabolic effects. J Cachexia Sarcopenia Muscle. 2014.